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Effects of dexamethasone on the metabolic responses to mental stress in humans
Author(s) -
Seematter G.,
Battilana P.,
Tappy L.
Publication year - 2002
Publication title -
clinical physiology and functional imaging
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.608
H-Index - 67
eISSN - 1475-097X
pISSN - 1475-0961
DOI - 10.1046/j.1365-2281.2002.00409.x
Subject(s) - medicine , dexamethasone , endocrinology , insulin , hemodynamics , glucocorticoid , vasodilation , sympathetic nervous system , mental stress , blood pressure
The haemodynamic effects of the sympathetic nervous system (SNS) activations elicited by hypoglycaemia, acute alcohol administration, or insulin can be prevented by a pretreatment with dexamethasone in humans. This suggests a possible role of central corticotropin releasing hormone (CRH) release. Mental stress activates the SNS, and decreases systemic vascular resistances through a β‐adrenergic‐mediated vasodilation thought to involve vascular nitric oxide release. It also increases insulin‐mediated glucose disposal, an effect presumably related to vasodilation. In order to evaluate whether activation of SNS by mental stress is glucocorticoid‐sensitive, we monitored the haemodynamic and metabolic effects of mental stress during hyperinsulinaemia in healthy humans with and without a 2‐day treatment with 8 mg day –1 dexamethasone. Mental stress decreased systemic vascular resistances by 21·9% and increased insulin‐mediated glucose disposal by 28·4% without dexamethasone pretreatment. After 2 days of dexamethasone treatment, whole body insulin‐mediated glucose disposal was decreased by 40·8%. The haemodynamic effects of mental stress were however, not affected. Mental stress acutely increased insulin‐mediated glucose disposal by 28·0%. This indicates that mental stress elicits a stimulation of SNS through dexamethasone‐insensitive pathway, distinct of those activated by insulin, alcohol, or hyperglycaemia.